The path to fitness or to over-training

The path to fitness

Successful training is based on a delicate balance between stressing the body and allowing it to recover. In the short term stress leads to damage and impaired performance but provided there is adequate opportunity for recovery, the body’s response to the challenge is to not only repair the damage but to develop a greater capacity to withstand challenge in future. This is described as super-compensation but in everyday terms, it simply means the body becomes fitter.

The path to over-training

However, if there is inadequate opportunity for recovery, performance continues to deteriorate and the body enters a state of staleness described as overtraining, that can persist for many months. In the over-trained state many aspects of body physiology are prone to be disrupted though there is no single physiological measure that indicates over-training. It is probable that the processes that lead to overtraining involve local trauma to body tissues, excessive production of ‘stress’ hormones such as cortisol, and excessive production of other chemical messengers in the body such as cytokines that re-set the brain mechanisms that regulate the body. It is probable that the derangements of body chemistry in any one case depend on the nature of the initial stress; on the genetic constitution of the individual; and on that individual’s previous history of stress and adaptation.

The first steps on the path to fitness or over-training

For long-distance runners, there are two processes that are the most likely candidates for initiating the processes that lead to either fitness or overtraining. These are damage to muscle fibres produced by the eccentric contraction that occurs on each footfall, and the release of cortisol by the adrenal gland to promote the generation of glucose required to fuel a long run. Understanding these processes is likely to be the key to rationally designing a successful training program.

Catabolic effects of cortisol

When the body faces stress, the initial response is release of cortisol from the adrenal gland. Cortisol plays part in several of the body’s immediate self-protective strategies. Of particular relevance for the long distance runner is the process of gluconeogenesis – the generation of glucose to prevent a fall in blood glucose that would be a catastrophe for the brain, which is heavily reliant on glucose to fuel its operations. Cortisol promotes the release of glucose from glycogen stores in the liver. However cortisol can also promote the breakdown of protein to generate glucose. So unaccustomed long runs are likely to result in the sacrifice of muscle protein for the sake the short term maintenance of blood glucose. This breaking down of body constituents is known as catabolism.

Eccentric damage to muscles

The mechanisms of muscle damage during exercise are not fully understood. It is unlikely that processes such as lactic acid production due to anaerobic metabolism play a significant role. It might be that increased acidity interferes to a limited extent with some beneficial processes such as the generation of mitochondria, (as indicated by the study by David Bishop and colleagues (Medicine & Science in Sports & Exercise:Vol 40(5) Supplement p S33, 2008), discussed in my post on 21st April. However, a substantial amount of evidence indicates that lactate actually protects muscles (Cairns SP, Sports Med. Vol. 36(4):279-91, 2006) Another potential mechanism of damage is the production of free radicals,. These are reactive molecules with an unpaired electron that are formed during oxidative metabolism and can damage tissue, but so far the evidence suggests that free radical damage is on likely to be a serious issue for elderly runners. (I myself am in that group, but in the present discussion I do not want to confine myself to the challenges facing the elderly).

As discussed above, the catabolic effects of cortisol can also promote break-down of muscle. However, the most significant source of damage during running is likely to be simple mechanical trauma. During weight lifting, the eccentric activity involved in controlled lowering of the weight can produce dramatic disruption of the structural integrity of muscles, that far exceeds the damage caused during concentric lifting, even though concentric lifting requires more energy. Forcefully stretching a muscle as it is actively generating an opposing force simply tears many of the muscle fibres apart, producing the pattern known as Z-line streaming (Gibala and colleagues, Journal of Applied Physiology, Vol 78, 702-708, 1995). Unfortunately, eccentric contraction occurs at each footfall during running, as the quads and calf muscles arrest the freefall under the influence of gravity that occurred during the airborne phase. Thus long distance running produces two potentially destructive effects: micro-trauma that tears the muscle fibres apart and the release of the catabolic hormone, cortisol, which acts in the short term to maintain blood glucose levels, but when the supply of glycogen in the lever is inadequate, is likely to breakdown muscle proteins to generate glucose. In the short term, muscle power suffers but in the medium term, these destructive processes can trigger adaptive responses that lead to greater fitness – provided the stress is not excessive. On the other hand, rapid increases in training volume leads to over-training and possible long term impairment of function, as was illustrated ib the study by Lehmann and colleagues discussed in my posting on 14th April (Int J Sports Med. Vol 12(5):pp 444-52, 1991; Br J Sports Med. Vol 26(4):pp 233-42, 1992; Eur J Appl Physiol Occup Physiol. Vol 70(5):pp 457-61, 1995).

The adaptive response to muscle damage

Several adaptive processes can occur. The two most important are closely linked: these are the mobilization of satellite cells and the production of anabolic hormones. Satellite cells are a form of stem cell that occur in muscle adjacent to the muscle fibrils. Following damage to the muscle, the satellite cells fuse with the muscle cells ( GE Adams, Satellite cell proliferation and skeletal muscle hypertrophy, Appl Physiol Nutr Metab. Vol 31, pp782-790, 2006). Muscle cells have multiple nuclei, containing the DNA and other molecular machinery necessary for initiating the synthesis of new proteins. When a satellite cell fuses with a muscle cell, it adds a new nucleus thereby enhancing the regenerative capacity.

Corticosteroid hormones can inhibit the action of satellite cells. This is most clearly established in the case of synthetic steroids such as prenisolone that are used for the treatment of autoimmune disorders (Betters and colleagues, Muscle & Nerve. Vol 37(2):pp 203-9, 2008). However, it would be expected that less potent naturally produced corticosteroids such as cortisol would have a similar, though perhaps less marked effect.

However, the hormonal regulation of metabolism entails not only the production of catabolic hormones such as cortisol that tend to break down body tissues, but also the production of anabolic hormones that promote the building up of body tissues. The most potent of these are the sex steroids, especially testosterone (though oestrogen also has anabolic effects). Vigorous muscular contraction promotes the release of testosterone (Grandys and colleagues, J Physiol Pharmacol. Vol 59 Suppl 7:89-103, 2008). Testosterone promotes the action of satellite cells.

The adrenal cortex also produces anabolic hormones of which DHEA (dihydroepiandrosterone) is the most abundant. DHEA is a multifunctional hormone, and its role in adaptation to training is uncertain. The question of whether DHEA supplements have a beneficial effect on muscle building has been a subject of some controversy. Less controversial are the beneficial anabolic effects of growth hormone. Growth hormone is produced by the pituitary gland and stimulates the building up of body tissues. The production of growth hormone is promoted by vigorous exercise, but the peak release of growth hormone occurs during sleep. Almost certainly, adequate sleep is required to promote the optimum switch from production of the catabolic hormone cortisol (which usually reaches its lowest level 3-5 hours after onset of sleep) to the production of growth hormone.

Failure of adaptation

If the amount of time for recovery is inadequate to allow the repair of muscle fibres and the re-synthesis of glycogen, a vicious cycle sets in. The damaged muscle tissue release cytokines which are small molecules that carry out various signaling functions in the body. Although the details remain speculative, it is likely that the cytokines produced by muscle damage act in the hypothalamus and in other regions of the brain to re-set the regulatory mechanisms that control the various physiological processes in the body (Smith LL,.J Strength Cond Res. Vol. 18(1):pp 185-93, 2004). In particular, the regulatory mechanisms are likely to shut down body functions that might promote further damage. In other words, your brain will not allow you to run far or fast. Cortisol production initially remains high, though eventually it is likely to fail. Anabolic steroid production falls. You will feel stale, de-motivated and possibly even depressed. You are now over-trained and it may be many months before your brain lets you engage in potentially destructive activities such as racing at your best level.

What are the lessons?

This brief (and somewhat speculative) exploration of modern molecular biology confirms what has been discovered by observant athletes and coaches over the years. The simplistic explanations such as the presumed damaging effects of lactate suggested by coaches such as Arthur Lydiard are probably wrong, but many of Lydiard’s observations of what works in practice are probably correct. However a thorough understanding of the molecular biology might allow a somewhat more effective application of the principles.

A few specific points that might be gleaned from the discussion above are:

1) long training runs are potentially beneficial as they provide an enough stress to produce appreciable muscle damage and appreciable cortisol production.

2) Rapid increase in training volume is likely to lead to over-training. On the other hand, if the build up of training volume occurs slowly, the adaptive processes will result in an increased capacity to cope with the stress of heavier training and in turn, to reap greater benefits.

3) Cross training employing a training mode that minimizes eccentric contractions (e.g. elliptical cross training; cycling or swimming) will allow a greater total training load at any given level of fitness, and in particular, might facilitate other valuable adaptations (e.g. increase in blood volume; increased cardiac stroke volume; increased ability to generate glucose from lactate in the liver) without triggering the cytokines that signal to the brain that it further training should be inhibited.

4) Adequate periods of recovery are essential and in particular, adequate sleep is crucial during period of heavy training.

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7 Responses to “The path to fitness or to over-training”

With ‘mechanical trauma’, I expect in running this can be reduced somewhat by running on soft surfaces (dirt, grass). Also, I wonder if the ‘marathon shuffle’ typically used by ultra runners helps? No doubt that elliptical cross-training is helpful in this regard.

Also, interesting about the value of sleep (growth hormone being released during sleep). I wonder if naps help, or just longer nightly sleeps – say 9 hours instead of 7?

Ewen, thanks for your comments. I would expect that the damage of eccentric contraction will be greatly reduced by the ultra-marathon shuffle. However, I do not think it is helpful to use the ultra-marathon shuffle in training for any event in which running fast is a more important objective than merely lasting the distance. Getting airborne is what does the damage when running but it is also what makes running so efficient. Efficient running requires spending as short a period on stance as the legs can cope with. I believe that the most important goal of endurance training is training the legs to cope with a short time on stance (and the associated eccentric contraction) safely. In my opinion, spending more than half of the gait cycle on stance encourages an inefficient style. If an athlete wants to cover more miles than he/she can handle safely when spending no more than half the gait cycle on stance, I think power walking would be a better use of time. This might produce as much aerobic development while saving up the weekly ‘damage allowance’ for more efficient running with a shorter time on stance.

As for naps, I doubt that occasional naps would be any where near as effective as a good night’s sleep for promoting anabolic effects, because the switch from catabolism to anabolism during sleep is facilitated by the body’s circadian rhythm. I suspect that much of the stress of jet lag is due to lack of synchrony between sleep and the body’s circadian rhythm.

The fact that some cultures have developed the tradition of siesta makes me wonder whether a regular daytime nap would create a circadian rhythm in which catabolism switches to anabolism during the siesta. On the other hand, there might be some benefits in letting the cortisol level remain high for a few hours after heavy exercise because cortisol would tend to suppress inflammation due to tissue damage. In the medium term, inflamation promotes recovery but too much inflamation does damage. Getting the balance right with steroid hormones (either natural or synthetic) is a tricky business. Ultimately it is very difficult to predict the full consequences of changes in training and life-style – so ‘listening to the body’ is crucial.

Andrew, Thanks. I had been pleased to read that you had been gradually building up the running again in recent weeks, and was sorry to read about the recent set-back with your knee. Once you are able to run and ride again, I hope you are able to enjoy a large amout of cycling and a very slow increase in the amount of running. The fact that the doctor recommended a cortisone injection for your knee empahsizes the complex interation between catabolic effects and anabolic effects. Cortisone (like cortisol) is catabolic and long term use would result in weakening of the tissues of your knee. However in the short term it helps suppress inflammation and promotes recovery – it can be magic for a wonky knee.

Thanks Canute for a really interesting article, I would just like to comment on eccentric muscle damage in running.
First I feel that it should not be thought as negative to put your running muscles through a hard eccentric workout ie fast downhill running, carried out say twice per month, infact such training can help the muscle deal with the trauma of a marathon, also I would recommend that not all your running should be done on soft surfaces [unless you plan to only trail race] the unaccustomed shock of racing on the road could lead to serious injury!
Thanks for your comments on my marathon greatly appreciated!
I’m very excited about trying to push the age v performance levels back, k through correct training and correct biomechanics!
CHEERS RICK

P.S, YES I USED THE SPIRA SHOES IN THE MARATHON.
They felt really good, only slight sciatic problem in the last few miles [ right foot starting to tighten up] but much better than any shoe I have worn before.
The after effects, mon, tue, sore calf muscles are the only after effects, no back or quad problems, will start easy running again later today!